CC16 alleviates PM2.5-induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosis.

IF 6.2 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES
Aili Wang, Jianling Liu, Zhangwen Li, Ze Qian, Shuo Yang, Shaohua Luo, Jinle Lin, Jian Wu
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引用次数: 0

Abstract

Background: Exposure to PM2.5 represents a significant public health challenge, closely associated with the worsening of asthma, a condition that still lacks effective preventive measures. Club Cell 16 kDa protein (CC16), recognized for its anti-inflammatory and antioxidant properties, may serve a protective function in asthma exacerbated by PM2.5; however, the underlying mechanisms, particularly those related to ferroptosis, remain poorly understood.

Methods: The impact of CC16 on inflammation and ferroptosis was assessed using a TC-1 lung epithelial cell model exposed to PM2.5, as well as an ovalbumin (OVA)-induced asthmatic mouse model also subjected to PM2.5 exposure.

Results: CC16 significantly modulated key regulators of ferroptosis (NRF2, GPX4, SLC7A11, HO-1) and attenuated pro-inflammatory cytokines (IL-13, IL-5, IL-6, IL-1β, IL-17A) in PM2.5-exposed lung epithelial cells. Furthermore, it enhanced pulmonary function while reducing airway inflammation and mucus secretion and inhibited ferroptosis in PM2.5-induced asthmatic mice.

Conclusion: CC16 demonstrates promise as a therapeutic agent for PM2.5-induced asthma by modulating ferroptosis and alleviating airway inflammation, thereby providing a novel strategy for asthma management.

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来源期刊
CiteScore
12.10
自引率
5.90%
发文量
1234
审稿时长
88 days
期刊介绍: Ecotoxicology and Environmental Safety is a multi-disciplinary journal that focuses on understanding the exposure and effects of environmental contamination on organisms including human health. The scope of the journal covers three main themes. The topics within these themes, indicated below, include (but are not limited to) the following: Ecotoxicology、Environmental Chemistry、Environmental Safety etc.
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